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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The study of the biochemical and physiological functions of the enkephalinergic cell has greatly extended our understanding of peptidergic cells in general. In the adrenal gland, the major part of the proenkephalin-derived peptides is present as intermediates in the processing of the precursor. These peptides are contained within the adrenergic chromaffin granules, from which they are released in response to stimulation of the cell. The nature of the products released depends on the nature of the stimulus, but it appears that mature granules containing completely processed peptides are preferentially released under physiological conditions. In the brain, the presence and release of the heptapeptide that comprises the carboxyl terminus of adrenal proenkephalin suggest that similar mechanisms are operating centrally. The identity of brain and adrenal proenkephalin is further supported by the purification from brain of a large fragment of the proenkephalin molecule, synenkephalin , and the occurrence in brain of this and the other proenkephalin-derived peptides in a molar ratio close to that found in the sequence of the adrenal precursor. The processing of proenkephalin in brain appears to follow the classical models first proposed for peptide hormones (Steiner et al. 1980), which may thus be generalized to include peptide neurotransmitters/neuroregulators. In addition, the results presented in this paper indicate that enkephalins may be cotransmitters in at least two diverse systems. Enkephalins and catecholamines are colocalized in the adrenergic granules of the adrenal gland. In the brain, enkephalins and oxytocin are colocalized in the magnocellular neurons of the hypothalamo-neurohypophyseal oxytocinergic pathway. In both of these systems, the enkephalins are present in a molar concentration that is less than 1% of the concentration of the principal messenger. Such colocalization , coupled with the numerous active peptides that may arise from proenkephalin, suggests many elegant but complex schemes of neurotransmitter interactions. For example, release of enkephalins in the neurohypophysis may regulate oxytocin release through an action on autoreceptors of the oxytocinergic terminal. In the adrenal the coreleased enkephalins may act by regulating presynaptically the cholinergic output of the splanchnic nerve. However, further studies are needed to define clearly the physiological roles of such cotransmission . From the abundance of proenkephalin-derived peptides in the basal ganglia, it appears that enkephalins may represent the principal transmitter in some central neurons.(ABSTRACT TRUNCATED AT 400 WORDS)
Cold Spring Harb Symp Quant Biol 1983
PMID:The enkephalinergic neuron: implications of a polyenkephalin precursor. 658 60

Congenital adrenal hyperplasia due to 21-hydroxylase deficiency is common in certain regions of the world characterised by cold winters. The persistence of this potentially lethal recessively inherited disease suggests that an evolutionary advantage is conferred upon the partially affected heterozygotes. Profound hypothermia following acute cold exposure in normal subjects carries a considerable mortality especially from cardiac arrhythmias and dehydration. A hypothesis is proposed to suggest that the incomplete block at the 21-hydroxylase step of steroid biosynthesis decreases stress-induced steroid responses, especially in the younger heterozygote and clinically non-salt-losing homozygote; glucocorticoid and mineralocorticoid insufficiency reduces the severity of cold-induced water diuresis; prevention of severe dehydration contributes towards the ability to survive profound hypothermia. Studies into the salt and water metabolism of the congenital adrenal hyperplasia heterozygote at various ages as well as examination of antidiuretic hormone and steroid hormone interactions upon the renal tubule in cold-exposed normal individuals are merited.
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PMID:Cold stress and congenital adrenal hyperplasia heterozygotes. 664 15

Filtered proteins including insulin are absorbed in the proximal tubule by means of pinocytosis. The first step in this process is binding of the protein to brush border membrane. As it is not known whether absorption exhibits specificity, we set out to determine whether specific binding sites for insulin are present in brush border membranes. Rabbit-isolated brush border membranes were incubated with 125I-insulin and varying concentrations of cold insulin or other peptide hormones. Binding and degradation of 125I-insulin occurred in a time- and temperature-dependent manner. Native insulin competitively inhibited 125I-insulin binding, but calcitonin, arginine vasopressin, glucagon, and growth hormone (10(-6) M) were relatively ineffective. Nonspecific binding averaged one-third of the total radioactivity bound. Scatchard analysis of binding data revealed two classes of insulin receptors: high affinity, low capacity receptors and low affinity, high capacity receptors. Gel filtration analysis of 125I-insulin exposed to brush border membrane revealed the formation of low-molecular-weight products similar to that produced by intact kidneys. The degrading process exhibited some specificity, for cold insulin (10(-6) M) was more effective than calcitonin, vasopressin, glucagon, or growth hormone in inhibiting degradation (32% versus less than 13% inhibition; P less than 0.01). Whether this reflects inhibition of insulin specific binding before exposure to degradation or inhibition of specific enzymes is unclear. In summary, it appears that renal brush border membranes have a major insulin-specific receptor component that could potentially mediate tubular insulin absorption. In addition, there is a smaller nonspecific component that may also have the potential to mediate insulin absorption. Finally, it appears that brush border membranes have the ability to degrade insulin to low-molecular-weight products by a process that exhibits some specificity for insulin.
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PMID:Binding and degradation of insulin by isolated renal brush border membranes. 676 Dec

Membrane fluidity, urea permeability, and osmotic water permeability in toad urinary bladder are regularly enhanced by antidiuretic hormone (ADH). In addition, organized intramembranous particle aggregates, which correlate specifically with hormonally stimulated water permeability, are found in granular cell luminal membranes consequent to ADH stimulation. In this investigation ADH-stimulated changes in urea and osmotic water permeability and luminal membrane aggregates at room temperature (24.8 +/- 0.4 degrees C) and in the cold 10.6 +/- 0.2 degrees) were compared with corresponding changes in membrane fluidity, as assessed by n-butyramide permeability. Although a critical level of membrane fluidity is undoubtedly required, the occurrence of aggregates in the luminal membrane is independent of an accompanying hormonally induced change of membrane fluidity. ADH-stimulated osmotic water permeability in toad bladder is also independent of the coincident change in membrane fluidity, and as a process almost certainly involves membrane channels, not a solubility-diffusion process through membrane lipids. For ADH-stimulated transbladder urea movement, channels seem to be involved as well, and the change induced in membrane fluidity by ADH could be an underlying factor in their formation.
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PMID:Relation of ADH effects to altered membrane fluidity in toad urinary bladder. 677 39

A radioimmunoassay for arginine-vasopressin in human plasma with use of a commercially available antibody was developed and evaluated. The hormone was extracted from plasma with cold 98% ethanol, which showed a significantly higher (p less than .001) and more precise recovery than with the acetone-ether procedure (65.3 +/- 3.7% vs 50.8 +/- 6.0%, respectively). The sensitivity was 0.31 pg per tube. Results for normal subjects in different physiological conditions and in patients with diabetes insipidus and inappropriate antidiuretic hormone secretion showed the good reliability of the method.
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PMID:Radioimmunoassay for arginine-vasopressin in cold ethanol extracts of plasma. 683 73

The effect of fusaric acid (FA) on the body temperature of age-matched spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto rats (WKY) was investigated at an ambient temperature of 4 degrees C. During a 7 h period of cold exposure the body temperature decreased by 6.5 degrees C in WKY (p less than 0.01) and by 5.4 degrees C in SR (p less than 0.05) after administration of 100 mg/kg FA, with the effects occurring faster in WKY. At 50 mg/kg the effect was lower. Naloxone completely abolished the temperature effect of FA in both rat strains. The naloxone antagonism may point to an opiate involvement in the thermoregulation after FA. A possible contribution of vasopressin and tetrahydroisoquinoline alkaloids to the maintenance of body temperature is also discussed.
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PMID:Effect of fusaric acid on the body temperature in spontaneously hypertensive and normotensive rats. 688 9

This patient demonstrates that peripheral vascular ischemia and gangrene may complicate the use of intraarterial vasopressin in the absence of catheter-related phenomena such as microemboli or catheter dislodgement. Discontinuation of vasopressin effectively reverses ischemic changes. Sympathetic blocking agents or direct-acting vasodilators may accelerate the reversal of the vasopressin induced ischemia. In the patient with a history of previous extremity cold injury, vasopressin may precipitate severe ischemia or gangrene by its direct effect at the arteriolar level in an extremity with already increased sympathetic vascular tone. Peripheral circulatory status must be assessed frequently during vasopressin infusion especially in patients with a history of frostbite.
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PMID:Upper extremity gangrene secondary to superior mesenteric artery infusion of vasopressin. 697 39

Plasma catecholamines and vascular response to noradrenaline were studied in phosphate depleted rats. Phosphate depletion was induced in rats by dietary phosphorus deprivation for 6 weeks. Basal plasma concentrations of noradrenaline, adrenaline and dopamine were elevated in phosphate depleted rats compared to pairfed control rats. After exposure to cold (4 degrees C, 45 min) the rise in plasma catecholamines was much more pronounced in phosphate depleted rats. In the isolated perfused rat heart, the uptake of tritiated noradrenaline was unchanged. In the isolated perfused hindlimb preparation the vascular response to noradrenaline, but not to potassium chloride and arginine-vasopressin was significantly diminished in phosphate depleted rats. It is concluded that in phosphate depletion sympathetic activity is elevated and vascular response to noradrenaline diminished.
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PMID:Dysfunction of the adrenergic system in phosphate depleted rats. 717 75

The purpose of this study was to determine if there is an interaction between carotid baroreceptors (CBR) and cardiopulmonary receptors with vagal afferents (CPVA) in the control of plasma vasopressin (ADH). Changes in ADH (radioimmunoassay) in the superior vena cava were determined in 13 chloralose-anesthetized dogs with aortic nerves sectioned during concomitantly induced changes in CBR and CPVA input. CBR input was changed by altering pressure (CSP) in the isolated perfused sinuses. Carotid sinus pressure (CSP) was initially set at 50 mmHg. The CPVA input was reversibly interrupted by cooling the vagi to 0 degrees C while CSP was concomitantly increased to 135 or 200 mmHg or was held constant at 50 mmHg. Vagal cold block (VCB) with CSP held constant at 50 mmHg resulted in large increases in arterial pressure and plasma vasopressin. Increases in CSP to 200 mmHg resulted in significant decreases in arterial pressure and in plasma vasopressin despite concomitant VCB. VCB and concomitant increase in CSP to 135 mmHg resulted in a significant fall in arterial pressure, whereas plasma vasopressin tended to increase. Thus, the influence on arterial pressure of raising CSP to 135 mmHg exceeds that of VCB. In contrast, the influence of VCB on ADH equals or exceeds that of raising CSP to 135 mmHg. These differential responses of arterial pressure and plasma ADH suggest an interaction between CBR and CPVA in the control of ADH and arterial pressure.
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PMID:Interaction between carotid and cardiopulmonary baroreflexes in control of plasma ADH. 728 51

The influence of various ulcerogenic treatments on healing gastric ulcers induced by thermocautery was studied in mice. A low dose of serotonin (5HT) which did not produce ulceration, was found to aggravate gastric ulcers at 15th or 30th day after thermocauterization, but other ulcerogenic treatments including histamine, norepinephrine, vasopressin, acetic acid ingestion and cold-restraint stress did not affect this induced gastric ulcer. Bleeding and ulceration, however, occurred in the gastric glandular portion in addition to thermocauterization ulcer by the treatment of acetic acid ingestion or cold-restraint stress. Histological sections of gastric ulcers (15th and 30th day) 24 hr after 5HT injection, showed severe necrosis of the regenerated mucosal layer. Microvessel structure in the gastric mucosa as revealed by the Indian-ink infusion, showed a local obstruction of blood flow on the edge of ulcers 1 or 3 hr after 5HT injection. Although acetic acid ingestion increased transmucosal fluxes of Na+ and K+, 5HT had no effect on the ion flux in normal mice. Thus the healed ulcer area was resistant to various ulcerogenic stimulants, except for 5HT, and the vasoactive factor of 5HT may be involved in the aggravating process of gastric ulcers induced by thermocautery.
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PMID:Aggravating effect of serotonin on gastric ulceration induced by thermocautery under the healing process in mice. 745 84


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